Delpre G, Grinblat J, Kadish U, Livni E, Shohat B, Lewitus Z, Joshua H
Am J Med Sci. 1979 Mar-Apr;277(2):207-13. doi: 10.1097/00000441-197903000-00010.
Jaundice with evidence of hepatocellular damage of moderate severity was observed in a patient who received methyldopa. The diffuse mononuclear infiltration of the liver tissue was found to consist of 90% E-rosette-forming cells. Peripheral lymphocytes gave a markedly positive macrophage migration inhibition (MIF) test against methyldopa. The number of T lymphocytes in the peripheral blood was at the lower limit of normal but they proved to be functionally inactive, as demonstrated by the results of a local xenogeneic graft-vs-host reaction test. The liver disease was associated with hyperglobulinemia, a decrease of the third and fourth components of complement and the presence of incomplete erythrocytic antibodies, leukoagglutinins, antinuclear factor, and smooth muscle antibody. Follow-up after discontinuation of the drug revealed a gradual return to normal of liver function and MIF tests, normalization of cellular immunity, and disappearance of the humoral antibodies. It is assumed that sensitization by methyldopa triggered the autoaggressive phenomena and their ultimate manifestation in the liver.
在一名接受甲基多巴治疗的患者中观察到黄疸伴有中度严重程度的肝细胞损伤证据。发现肝组织的弥漫性单核细胞浸润由90%的E花环形成细胞组成。外周淋巴细胞对甲基多巴的巨噬细胞游走抑制(MIF)试验呈明显阳性。外周血中T淋巴细胞数量处于正常下限,但如局部异种移植物抗宿主反应试验结果所示,它们被证明功能无活性。肝脏疾病与高球蛋白血症、补体第三和第四成分减少以及不完全红细胞抗体、白细胞凝集素、抗核因子和平滑肌抗体的存在有关。停药后的随访显示肝功能和MIF试验逐渐恢复正常,细胞免疫正常化,体液抗体消失。推测甲基多巴致敏引发了自身攻击现象及其在肝脏中的最终表现。